Folwaczny E K, Stürmer K M
Klinik für Unfallchirurgie, Plastische und Wiederherstellungschirurgie, Universitätsklinikum, Zentrum Chirurgie, Georg-August-Universität Göttingen.
Chirurg. 1999 May;70(5):588-93; discussion 593-4. doi: 10.1007/s001040050691.
We report a truck driver with severe soft tissue contusion of both legs who developed atypical heparin-induced thrombocytopenia (HIT) after a thrombosis prophylaxis with unfractionated heparin; despite a thrombosis the patient showed a systemic allergic reaction to heparin in combination with elevation of thrombocytes and positive heparin-dependent antibodies. Six days after the initial trauma deep vein thrombosis of the left lower leg was diagnosed and fasciotomy was performed, preventing an imminent compartment syndrome. Another 5 days later the patient developed exanthema of the trunk and upper extremities and urticaria on his face, as well as severe headache. His platelet count increased from 134,000/microliter to 258,000/microliter. After exclusion of other causes for these symptoms, a reaction to heparin-dependent antibodies (heparin-platelet-factor 4 complex) was demonstrated 2 days later. Thrombosis prophylaxis was changed to hirudin (Refludan) and elevation of thrombocytes to 445,000/microliter was noted. Shortly after rinsing of an intravenous line with less than 50 IE unfractionated heparin at day 36 after trauma the patient developed an anaphylactic shock, which could be managed with cortisone. We suggest that in HIT the thrombocytopenia may represent only one form of an allergic reaction to heparin. The cause of the thromboembolic event is an antigen-antibody reaction to heparin taking place on the surface of the thrombocyte. This is similar in all forms of systemic reaction to heparin application, even though the symptoms may vary. As thrombocytopenia may not be the main symptom of a heparin-induced antibody reaction--in our hospital only 5 of 10 patients with HIT--the disease should rather be named "heparin allergy". We suggest a new classification of different pattern of heparin allergy types I-IV. The new types I and II are similar to HIT types I and II. Type III is the reaction of antibodies without decrease of thrombocytes, and type IV the reaction of antibodies associated with systemic allergic symptoms.
我们报告一例双腿严重软组织挫伤的卡车司机，其在接受普通肝素血栓预防治疗后发生非典型肝素诱导的血小板减少症（HIT）；尽管存在血栓形成，但患者出现了对肝素的全身过敏反应，同时伴有血小板升高和肝素依赖性抗体阳性。初始创伤6天后，诊断为左下肢深静脉血栓形成并进行了筋膜切开术，预防了即将发生的骨筋膜室综合征。又过了5天，患者出现躯干和上肢皮疹、面部荨麻疹以及严重头痛。其血小板计数从134,000/微升增至258,000/微升。在排除这些症状的其他病因后，2天后证实为对肝素依赖性抗体（肝素 - 血小板因子4复合物）的反应。血栓预防治疗改为水蛭素（Refludan），并注意到血小板升至445,000/微升。创伤后第36天，在使用少于50国际单位普通肝素冲洗静脉管路后不久，患者发生过敏性休克，可通过使用皮质激素进行处理。我们认为在HIT中，血小板减少症可能仅代表对肝素过敏反应的一种形式。血栓栓塞事件的原因是血小板表面发生的针对肝素的抗原 - 抗体反应。这在所有肝素应用的全身反应形式中都是相似的，尽管症状可能有所不同。由于血小板减少症可能不是肝素诱导抗体反应的主要症状——在我们医院10例HIT患者中仅有5例——该疾病更应命名为“肝素过敏”。我们建议对肝素过敏I - IV型的不同模式进行新的分类。新的I型和II型类似于HIT的I型和II型。III型是无血小板减少的抗体反应，IV型是与全身过敏症状相关的抗体反应。
